Importance of promoter methylation of GATA4 gene in epithelial ovarian cancer

被引:14
|
作者
Chmelarova, Marcela [1 ,2 ]
Dvorakova, Eva [2 ,3 ]
Spacek, Jiri [2 ,3 ]
Laco, Jan [2 ,4 ]
Palicka, Vladimir [1 ,2 ]
机构
[1] Charles Univ Prague, Fac Med Hradec Kralove, Inst Clin Biochem & Diagnost, Hradec Kralove, Czech Republic
[2] Univ Hosp Hradec Kralove, Hradec Kralove, Czech Republic
[3] Charles Univ Prague, Fac Med Hradec Kralove, Dept Obstet & Gynecol, Hradec Kralove, Czech Republic
[4] Charles Univ Prague, Fac Med Hradec Kralove, Fingerland Dept Pathol, Hradec Kralove, Czech Republic
来源
BIOMEDICAL PAPERS-OLOMOUC | 2013年 / 157卷 / 04期
关键词
methylation; GATA4; ovarian cancer; epigenetics; TRANSCRIPTION FACTORS; EXPRESSION; HYPERMETHYLATION;
D O I
10.5507/bp.2013.079
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Aims. Ovarian cancer is the most lethal gynecological malignancy, with typically late diagnosis. Altered DNA methylation of tumor suppressor gene promoters probably plays a relevant role in ovarian carcinogenesis and frequently occurs as an early event in the development of different types of cancer including ovarian carcinoma. GATA4 methylation has been reported in a variety of human cancers. The aim of this study was to investigate promoter methylation of the GATA4 gene in ovarian cancer by comparison with that in normal ovarian tissue. Methods. To search for promoter methylation of the GATA4 gene we used MSP (methylation-specific PCR) to compare the methylation status in 67 tissue samples of ovarian cancer with that in 40 control samples. Results. In our study, methylation-specific PCR revealed GATA4 promoter methylation in 21 of 67 specimens with ovarian cancer (31.3%), and in none of the control ovarian tissue samples. Conclusion. These results confirm that methylation in the GATA4 promoter region could play an important role in ovarian carcinogenesis, and show new loci which are highly methylated only in ovarian cancer samples and which are associated predominantly with the endometrioid type of ovarian carcinoma.
引用
收藏
页码:294 / 297
页数:4
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